Cited by 247Cancer Risks and FactorsAdipokines, Inflammation, and Metabolic DiseasesCancer, Lipids, and Metabolism

Visceral adiposity, insulin resistance and cancer risk

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Donohoe, Claire L, Doyle, Suzanne L, Reynolds, John V·2011·Diabetology & Metabolic Syndrome

Abstract

BACKGROUND: There is a well established link between obesity and cancer. Emerging research is characterising this relationship further and delineating the specific role of excess visceral adiposity, as opposed to simple obesity, in promoting tumorigenesis. This review summarises the evidence from an epidemiological and pathophysiological perspective. METHODS: Relevant medical literature was identified from searches of PubMed and references cited in appropriate articles identified. Selection of articles was based on peer review, journal and relevance. RESULTS: Numerous epidemiological studies consistently identify increased risk of developing carcinoma in the obese. Adipose tissue, particularly viscerally located fat, is metabolically active and exerts systemic endocrine effects. Putative pathophysiological mechanisms linking obesity and carcinogenesis include the paracrine effects of adipose tissue and systemic alterations associated with obesity. Systemic changes in the obese state include chronic inflammation and alterations in adipokines and sex steroids. Insulin and the insulin-like growth factor axis influence tumorigenesis and also have a complex relationship with adiposity. There is evidence to suggest that insulin and the IGF axis play an important role in mediating obesity associated malignancy. CONCLUSIONS: There is much evidence to support a role for obesity in cancer progression, however further research is warranted to determine the specific effect of excess visceral adipose tissue on tumorigenesis. Investigation of the potential mechanisms underpinning the association, including the role of insulin and the IGF axis, will improve understanding of the obesity and cancer link and may uncover targets for intervention.

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Research works printed but not linked: 3

  1. Calle EE Kaaks R Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms Nat Rev Cancer 2004 579 591 15286738
  2. Wajchenberg BL Subcutaneous and Visceral Adipose Tissue: Their Relation to the MetabolicSyndrome Endocr Rev 2000 21 697 738 10.1210/er.21.6.697 11133069 · DOI · Paper page
  3. Giovannucci E Metabolic syndrome, hyperinsulinemia, and colon cancer: a review The American Journal of Clinical Nutrition 2007 86 836S 842S 18265477

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Authors
Donohoe, C. L., Doyle, S. L., & Reynolds, J. V.
Affiliations
Trinity College Dublin (IE)
Corresponding author
Reynolds, John V
Venue
Diabetology & Metabolic Syndrome
Published
2011-06-22
Volume
3
Issue
1
Pages
12-12
ISSN
1758-5996 (ISSN-L)
OpenAlex
W2119964718
Cited by
247
References
182
Citations by year
2026: 8 · 2025: 16 · 2024: 14 · 2023: 16 · 2022: 14 · 2021: 16 · 2020: 22 · 2019: 29 · 2018: 14 · 2017: 15 · 2016: 17 · 2015: 11 · 2014: 19 · 2013: 15 · 2012: 19
FWCI
8.67
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Diabetology & Metabolic Syndrome (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Arrow@dit (Dublin Institute of Technology) (submittedVersion, cc-by-nc-sa)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • Lenus, The Irish Health Repository (Dr Steevens Hospital Library) (submittedVersion)
Funders
  • Irish Cancer Society
  • Irish Research Council for Science, Engineering and Technology
  • Irish Research Council
Topics
  • Health Sciences › Medicine › Oncology › Cancer Risks and Factors
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
Keywords
visceral fat, obesity, cancer risk, insulin resistance, insulin-like growth factor axis, adipose tissue endocrine function, adipokines, sex steroids, chronic inflammation, paracrine effects, carcinogenesis, tumor progression

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